APSF NEWSLETTER Summer 2008

PAGE 32

Letter to the Editor

Modified Calculation of the Cerebral Perfusion Pressure in a Sitting Position: Jugular Starling Resistor and Related Clinical Implications
To the Editor:
Recent case reports described permanent injury from global cerebral ischemia in a beach chair position.1,2 Follow-up discussion in the APSF Newsletter did not result in consensus on safe limits of arterial blood pressure during anesthesia in the sitting position, how the blood pressure should be measured during head-up tilt, and the beta-blockers role in these complications.3,4 Cases of cerebral ischemia in a beach chair position mandate the revision of postural cerebral perfusion management. Perfusion pressure is the difference between the inflow Pi and outflow pressure Po, measured at the organ level: CPP=MAP-CVP or CPP=MAP-ICP if ICP>CVP. While measuring pressure in the intercommunicating vessels, we have to account for the hydrostatic pressure difference (gh), where h is the difference in height between 2 measurement points and is the density of blood. Because of the energy conservation law, heart work against gravity is zero (blood flows in a circular fashion as described by Harvey and potential energy remains the same upon completion of the circle).5 Therefore the site of CPP measurement could be anywhere, as long as the hydrostatic gradient from the measurement site to the organ level remains the same for inflow and outflow pressures and there is no significant flow related pressure drop between the measurement site and the organ level.4 Simple addition of hydrostatic column from the measurement level to the organ level does not change CPP value: (MAP + gh) (CVP + gh) = MAP CVP. And yet so many neuroanesthesiologists continue to zero the arterial pressure transducer at the level of the external acoustic meatus.3 Several considerations come here into play: 1) Measuring arterial pressure alone does not define CPP. In the sitting position arterial pressure is different if measured at the head, torso, or calf level, while CPP is a pressure difference and remains the same. When the arterial pressure transducer drops on the floor, arterial hypertension can be falsely diagnosed. CPP = MAP CVP would stay the same whether measured at the head, torso, or the floor level. 2) The hydrostatic indifference level (HIL) is a point where pressure does not change during body tilt. Measuring MAP or (MAP CVP) at this level should be indifferent to the body tilt. The only problem with this approach is that HIL has to be individually determined and HIL for venous and arterial systems was found to be different due to the difference in regional compliances. 3) Even if we measure MAP and CVP simultaneously and eliminate the self-negating effect of hydrostatic column gh (25 cm water = 18 mmHg) from the brain to the measurement site, we can not reliably estimate CPP. Negative transmural pressure leads to jugular collapse with the headup tilt. Directly measured jugular pressure above the thoracic inlet in the upright position stayed around 0 mmHg despite negative CVP in 8 healthy subjects with a gradient reaching 20 cm of water. No such gradient was observed in 2 patients with chronic cardiac tamponade.6 4) Arterial pressure measured at the zero venous pressure level is arithmetically equivalent to cerebral perfusion pressure (CPP = MAP 0). Skull base approximates zero venous pressure level when CVP gh < 0, because jugular veins are exposed to the atmospheric pressure upon exiting the scull. This is the reason why we should adjust the site of arterial pressure measurement when sitting. That is why the skull base can be referred as zero venous pressure level for the cerebral perfusion pressure estimation, unless venous pressure is measured in the jugular bulb directly. 5) Assessing CPP and adjusting the BP measurement level from the heart to the skull (about 20 mmHg) may not be important if MAP is maintained >70100 mmHg (CPP >50-80), but it is critical if MAP is maintained at 50 mmHg (CPP 30 mmHg). Venous outflow depends not only on the outflow pressure, but also on the venous resistance. Veins tend to collapse when external pressure exceeds intraluminal pressure, and venous resistance correspondingly increases. Venous resistance becomes infinitely high during occlusion. This phenomenon can interchangeably be described by the nonlinear venous outflow resistance or the change in effective venous outflow pressure (Starling resistor). Starling resistor is implied in the classic definition of cerebral perfusion pressure (mean arterial pressure minus intracranial or venous pressure, whichever comes higher): CPP = MAP ICP, when ICP > CVP, and CPP = MAP CVP when CVP > ICP.4 Jugular veins are exposed to atmospheric pressure and collapse with the head-up position.6 This collapse can be directly observed when jugular vein distention (JVD - external jugular vein collapse point) moves with the body tilt. Complete cessation of flow in both jugular veins was observed in 2/23 healthy volunteers at 15 and in 9/23 at 90 head-up tilt.7 Pressure in jugular veins may become negative due to subtraction of the hydrostatic gradient gh from CVP. Therefore CPP = MAP Patm (0), whenever CVP gh < 0 and ICP < 0. Global brain ischemia during controlled hypotension in a beach chair position is a particular case of the cerebral venous steal.8 Cerebral ischemia develops because of exhausted cerebral autoregulation (beta blockade) and is exacerbated by the jugular venous collapse in the sitting position, which leads to a further reduction of CBF (cardiac output diversion or steal from the brain similar to the blood flow diversion toward dependent portions of pulmonary circulation). This phenomenon occurs in the sitting position during craniotomy, when CVP gh < 0 (Patm = ICP = 0 with open cranium) and can be accompanied by a venous air embolism if the non-collapsible venous sinus is injured. Cerebral venous steal due to jugular collapse can also occur in patients with intact cranium, when ICP 0 and CVP - gh << 0. Although the vertebral venous plexus becomes the predominant outflow pathway during jugular compression in the sitting position, 7 flow through it is impeded during head rotation/tilt, especially in patients with cervical stenosis. Thus the practice of CPP measurement site adjustment to the skull base level, whenever patient position is changed and CVP - gh < 0, is justified. If jugular bulb pressure can be measured directly, pressure transducer level adjustments do not affect CPP calculation, as long as both the arterial and venous transducers stay at the same level.9 Given the above considerations, we propose generalizing the CPP formula to account for the effect of atmospheric pressure on the jugular veins. In a sitting position the atmospheric pressure (Patm = 0) will become an effective outflow pressure whenever it exceeds venous pressure. Thus,
CPP = MAP ICP, CPP = MAP CVP, CPP = MAP Patm, if ICP>CVP and ICP>Patm if CVP>ICP and CVP>Patm if Patm>CVP and Patm>ICP (1) (2) (3)

(whichever results in the smallest difference). If measurements are done at a different level than the skull base or the head position is changed, the hydrostatic pressure gradient (gh) has to be subtracted from all the terms of the CPP equation except

See Calculation, Next Page

APSF NEWSLETTER Summer 2008

PAGE 33

Simple Considerations Proffered Letter to the Editor To Minimize Sitting Position Risks Reader Recommends
Calculation, From Preceding Page
from the atmospheric pressure, as atmospheric pressure does not change when adjusting the measurement level. If CVP is maintained above 18 mmHg (gh), the classical CPP definition1,2 is valid and measurement level adjustments are not mandatory. To minimize risk of unrecognized global cerebral ischemia in the sitting position we propose several simple considerations: 1) Obtain baseline BP measurement in the sitting position and use it as a guide (measurement site is not critical as long as it does not change during the case and central blood pressure pulse wave propagation/reflection remains similar). 2) Evaluate for signs of cervical stenosis; avoid cervical malpositioning which could impede blood outflow through the vertebral venous plexus. 3) Document any patient position changes and changes in BP measurement site or technique. 4) If patient position or BP monitoring site is changed, reassess the new CPP to account for the Starling resistor in the cervical veins (CPP = (MAP gh) max ((ICP gh), (CVP gh), Patm), whereas h is the height from skull base to BP measurement site, Patm=0. 5) Visual assessment of the jugular vein column predicts if jugular veins will collapse in the sitting position.10 6) Volume loading will counteract the effect of Patm on the jugular veins and will prevent their collapse once CVP > gh (about 18 mmHg). 7) If the controlled hypotension is prolonged and exceeds diurnal minimum in the upright blood pressure, consider neuromonitoring (regional technique, maintaining verbal contact, near infrared cerebral oximetry, MCA Doppler, EEG, etc.). Mindaugas Pranevicius, MD Osvaldas Pranevicius, MD, PhD Bronx, NY References
1. Cullen DJ, Kirby RR. Beach chair position may decrease cerebral perfusion; catastrophic outcomes have occurred. APSF Newsletter. 2007;22(2):25,27. 2. Pohl A, Cullen DJ. Cerebral ischemia during shoulder surgery in the upright position: a case series. J Clin Anesth. 2005;17:463-9 3. Cucchiara RF. Hazards of beach chair position explored. APSF Newsletter. 2008;22(4):81. 4. Munis J. The problems of posture, pressure, and perfusion: cerebral perfusion pressure defined. APSF Newsletter. .2008; 22(4):82-3. 5. Harvey W. On the motion of the heart and blood in animals. London: George Bell and Sons; 1889. 6. Avasthey P. Venous pressure changes during orthostasis. Cardiovasc Res. 1972;6:657-63. 7. Valdueza JM, von Munster T, Hoffman O, et al. Postural dependency of the cerebral venous outflow. Lancet. 2000;355:200-1. 8. Pranevicius M, Pranevicius O. Cerebral venous steal: blood flow diversion with increased tissue pressure. Neurosurgery. 2002;51(5):1267,73; discussion 1273-4. 9. Eckenhof JE, Enderby GE, Larson A, et al. Human cerebral circulation during deliberate hypotension and headup tilt. J Appl Physiol. 1963;18:1130-8. 10. Sinisalo J, Rapola J, Rossinen J, et al. Simplifying the estimation of jugular venous pressure. Am J Cardiol. 2007;100:1779-81.

Zero Tolerance
To the Editor:

First I would like to confer my support for the APSF. An open forum is the best way to discuss and solve safety issues. Second, it is good to see the APSF fund safety research initiatives. One hopes, the $1.092 million recently divided among a number of proposals will make a difference. I have to take umbrage with Dr. Asokumar Buvanendran's proposal Patients after Minor Surgery with MAC: Is It Safe to Drive? Is this research necessary, and does it pass a common sense test? Have we as a society minimized the attention we pay to driving safety well beyond what is reasonable? Would MADD (Mothers Against Drunk Driving) approve of this research? National Highway Traffic Safety Administration statistics for 2006 show that 42,642 people were killed and 2,575,000 people were injured in motor vehicle accidents for the previous 1-year period. Over 17,000 of the deaths were alcohol related. Blood alcohol content (BAC) research originally looked at BAC from .02% to 0.1% and found impairment was commonly seen at the .02% levels, but we have rather arbitrarily fixated on .08% as the safe BAC. Many other countries have set lower limits. Cell phones, GPS screens, eating, even in-dash video screens are the norm. Drunk driving and speeding is rampant. I jog, cycle, and motorcycle and am commonly a victim of driver inattention and distraction. Now I might have to worry about a driving, hungry, sleep deprived colonoscopy patient calling ahead his take-out food order on his cell phone! Dr. Buvanendran's proposal contends if we can return to a baseline level of weaving, reaction times, and collisions on a driving simulator we can drive home. Would he also contend that we are able to return to work safely as well? Should your surgeon, anesthesia provider, and nursing staff go back to work after sedation or a glass of wine at lunch? There should be NO double standard for driving performance and everything else. We as health care professionals should champion a zero tolerance of intoxicants while driving. William Higgins, CRNA Kaneohe, HI

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